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HOW TO READ A CTG

ABDULLAH ASAAD
6TH YEAR MEDICAL STUDENT
HASHEMITE UNIVERSITY

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Cardiotocography (CTG) is used during pregnancy to monitor both the fetal heart and
contractions of the uterus. It is most commonly used in the third trimester. Its purpose is to
monitor fetal well-being and allow early detection of fetal distress. An abnormal CTG
indicates the need for more invasive investigations and potentially emergency caesarian
section.

The heart beat originates in the sinoatrial node in the atrium and is controlled by the
autonomic nervous system, primarily the sympathetic and parasympathetic pathways.
Stimulation of the sympathetic pathway results in an increase in heart rate, whilst
stimulation of the parasympathetic system, via the vagus nerve, will cause a decrease in the
heart rate.
The sympathetic system matures at a quicker rate than the parasympathetic, therefore
exerting a stronger influence in the preterm fetus.

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HOW TO READ IT ??
1. CHECK THE NAME.
DR C BRAVADO
2. CHECK THE TIME AND THE DATE
DR Define Risk
3. DEFINE RISK AND THE INDICATION OF CTG . C Contractions
4. CHECK THE MATERNAL PULSE, TEMPERATURE BRa Baseline Rate
5. DRUGS IF ANY- PETHIDINE, BETAMETHASONE etc. V Variability
A Accelerations
6. CHECK YOUR PAPER SPEED FIRST ( 1CM/1MIN) . D Decelerations
7. BASELINE O Overall impression

8. VARIABILITY
9. ACCELERATIONS
10.DECELERATIONS

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Baseline fetal heart rate
This is estimated over a 510-minute period of CTG excluding accelerations or decelerations
and is recorded in beats per minute (bpm).
In normal circumstances the baseline fetal heart rate is 110160 bpm.

max160 bpm

min110 bpm

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Baseline bradycardia
Baseline bradycardia is defined as being a persistently low baseline of below 110 bpm.

Causes
Gestational age of greater than 40 weeks. Some post-term fetuses have a marked vagal tone,
causing a slowing of the heart rate, and can show a baseline bradycardia of 100110 bpm.
Cord compression. In cases of acute hypoxia and cord compression a change in heart rate can
be evident from within a normal range to a bradycardia that does not recover to the baseline.
Congenital heart malformations.
Certain drugs, e.g. Benzodiazepines ,narcotic ,sedation and epidural anesthesia.
Maternal hypothyroid.
Sleeping cycle (not more than 40 mm)
Maternal supine hypotension syndrome

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Baseline tachycardia
Baseline tachycardia is defined as being a persistently high baseline of above 160 bpm. A
baseline heart rate
Excessive fetal movements or fetal stimulation. ( If the fetus is very active during the period when the CTG is
being performed, the fetal heart may not be showing a true baseline. This should be classed as reactivity, but can be
mistakenly diagnosed as fetal tachycardia.)
Maternal stress and anxiety. If the mother is in a stressful situation, or has a high anxiety level, she
will release catecholamine, thereby stimulating the sympathetic nervous system, resulting in an increase in
both maternal and fetal heart rates.
Causes

Gestational age. (A fetus at a gestational age of 32 weeks or below can show a baseline tachycardia
due to the immaturity of the vagus nerve.)
Maternal tachycardia. This may be as a result of dehydration and/or ketosis leading to poor uterine
perfusion.
Maternal pyrexia. A maternal pyrexia of 37.5C or higher may indicate infection and possible
chorioamnionitis .
Fetal infection. During infection, oxygen requirements are raised. The heart rate rises to increase the
oxygen transfer around the body.
Fetal hypoxia. Chronic changes in the levels of oxygen tension in the blood and fetal tissues lead to an
increase in the sympathetic activity, resulting in a rise in heart rate. 7

Fetal hormones. (maternal hyperthyroid , epinephrine )


Bradycardia

Tachycardia
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Variability
The beat to beat changes in the heart rate. Normal variability is 525 bpm ,Variability <5
bpm is classed as reduced.
Variability occurs as a result of the interaction between the nervous system, chemoreceptors,
baroreceptors and cardiac responsiveness.

(any accelerations &


decelerations should
be excluded)

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Decreased variability
Fetal sleep. During fetal sleep the CTG commonly gives an appearance of decreased variability; The
pattern does not usually persist for longer than 40 minutes.
Administration of drugs to the mother. pethidine for pain relief in labour, or sedative drugs.
Gestational age. The CTG of a fetus at a gestational age of less than 3032 weeks may show decreased
variability, probably due to the immaturity of the autonomic nervous system.
Hypoxia.(Fetus acidosis) When the fetus is suffering from hypoxia the autonomic nervous system fails to
respond to stress and the changes in venous return and metabolic demands of the fetus.
Congenital heart abnormalities.
May seen in Fetal tachycardia.

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Sinusoidal pattern.
These patterns are identifiable by the smooth, undulating, sine wave-like baseline.
Chronic fetal anemia associated with erythroblastosis fetalis, usually from Rh sensitization
Acute, intrapartum asphyxia
Fetal-maternal hemorrhage
In-utero, fetal hemorrhage
This pattern may be a result of cord compression, resulting in alternating hypervolemia and hypovolemia, or
of a raised intraperitoneal pressure due to the presence of ascites.
A fetus with anemia, as a result of rhesus incompatibility, twin-to-twin transfusion or a large fetal
bleed such as ruptured vasa praevia, may produce a sinusoidal pattern, reflecting hypoxia.
This pattern can also be seen as a result of fetal thumb-sucking, and is sometimes seen following the
administration of narcotic analgesia, particularly pethidine, to the mother.

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Sinusoidal pattern.

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BASELINE FETAL HEART RATE BASELINE VARIABILITY
Reassuring: Reassuring:
110 to 160 beats/minute 5 to 25 beats/minute

Non-reassuring:
Non-reassuring:
Less than 5 bpm for 30 to 50 minutes
100 to 109 beats/minute
More than 25 bpm for 15 to 25 minutes
161 to 180 beats/minute
Abnormal:
Abnormal: Less than 5 bpm for more than 50 min.
Below 100 beats/minute More than 25 bpm for more than 25 min.
Above 180 beats/minute. Sinusoidal.
Although a baseline fetal heart rate intermittent periods of reduced baseline
between 100 and 109 beats/minute is a variability are normal, especially during periods
non-reassuring feature, continue usual of quiescence ('sleep').
care if there is normal baseline variability
and no variable or late decelerations.
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NICE Guidance
Feb 2017
Accelerations
An acceleration is an increase in the fetal heart rate of 15 bpm or more, lasting for at least
15 seconds.
Accelerations usually occur in response to either a fetal movement or a uterine contraction.
The presence of accelerations is reassuring.

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The presence of fetal heart rate accelerations, even with reduced baseline variability, is generally a sign that
the baby is healthy. NICE FEB 2017
Decelerations
Decelerations are an abrupt decrease in the baseline fetal heart rate of greater than 15 bpm for
greater than 15 seconds.
Decelerations of the fetal heart rate from the baseline can be classified into four types:
1. Early
2. Late
3. Variable
4. Prolonged.

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Early decelerations
Early decelerations tend to be uniform in shape and occur with each contraction. They
often appear in a mirror image of the contraction.
The onset of the deceleration is at the onset of the contraction.
The heart rate reaches its lowest point at the peak of the contraction and has
recovered to the baseline by the end of the contraction.
Caused by compression of the fetal head during a contraction. they are seen in late first stage of
labour. compression of the fetal head causes an increase in intracranial pressure and therefore a decrease in
cerebral blood flow and oxygenation. the decrease in oxygen tension is detected by cerebral
chemoreceptors, and parasympathetic activity is increased. during head compression, pressure on the vagal
centre in the brain may also occur, increasing parasympathetic activity.

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Late decelerations
Late decelerations are usually uniform in shape and depth and occur after each contraction. Any
deceleration whose lowest point occurs more than 15 seconds after the peak of the contraction is said
to be late.
Late decelerations arise as a result of a decrease in uterine blood flow and therefore oxygen transfer
during a uterine contraction. Uteroplacental-induced hypoxia
Causes
Any condition which causes a reduction in placental blood flow may result in late decelerations, for example:
Placental abruption
Maternal hypotension
Excessive uterine activity.
Any maternal or pregnancy-related disease which may result in placental pathology can also cause
late decelerations, for example:
Diabetes mellitus
Pre-eclampsia.

Any fetus that is already compromised, by either lack of intrauterine growth retardation
stored glycogen or a reduction in circulating red blood prematurity
cells for the transfer of oxygen, is also at an increased risk rhesus isoimmunization 19

of developing late decelerations: twin-to-twin transfusion.


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The presence of late decelerations is concerning and fetal blood sampling for pH is indicated. 21

If fetal blood pH is acidotic it indicates significant fetal hypoxia and the need for emergency C-section.
Variable decelerations
Variable decelerations are inconsistent in shape and frequency and in their relationship to
uterine contractions
They are common and most decelerations that occur in labour are variable.
Variable decelerations appear
to occur as the result of
transient compression of the
umbilical cord, between the
fetus and surrounding maternal
tissues or fetal parts, during a
uterine contraction.
Causes
Umbilical cord around the
neck or body
True knot in the umbilical cord
Prolapsed umbilical cord.
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During a uterine contraction, venous return is obstructed,
leading to a decrease in venous return to the fetal heart.
This in turn results in a decrease in cardiac output, and
therefore arterial pressure.
The baroreceptors in the aortic arch are stimulated and
sympathetic activity is increased, resulting in a rise in the
fetal heart rate to maintain the blood pressure. With further
cord compression, the arterial flow becomes obstructed
and fetal hypertension results.
The baroreceptors in the aortic arch are stimulated, this
time resulting in increased parasympathetic activity,
leading to a fall in the fetal heart rate.

The effect of variable decelerations upon the fetus varies


depending upon the duration and degree of cord
occlusion that occurs during a contraction.
Typical variable decelerations have shoulders (accelerations on
either side of the deceleration)
This demonstrates a normal physiological response to cord
compression and is a reassuring feature. 23
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Atypical variable decelerations are
more suggestive of fetal
compromise developing

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Prolonged deceleration
A prolonged deceleration is described as consisting of a drop in the fetal heart rate of 30 bpm or
more, lasting for a period of at least 2 minutes

Causes
Total umbilical cord occlusion, e.g. cord prolapse.

Maternal hypotension resulting from the


administration of local anesthetic via an epidural
catheter.

Uterine hypercontractility.

Prolonged decelerations can also be evident following


vaginal examination or artificial rupture of the
membranes. This could be due to direct pressure being
applied on to the fetal head, resulting in pressure on
the vagal center in the brain. 26
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Feature
Description Baseline (beats/ Baseline variability Decelerations
minute) (beats/ minute)
110 to 160 5 to 25 None or early
Reassuring
Variable decelerations Typical variable for less
than 90 minutes
100 to 109 Less than 5 for 30 to Typical variable decelerations with over
OR 50 minutes 50% of contractions, for over 90 min.
161 to 180 OR OR
Non-reassuring Single prolonged deceleration for up to 3 minutes
More than 25 for 15
to 25 minutes

Below 100 Less than 5 for more Either atypical variable decelerations
OR than 50 minutes with over 50% of contractions or late
Above 180 OR decelerations, both for over 30 minutes
More than 25 for Single prolonged deceleration for more
Abnormal more than 25 minutes than 3 minutes
OR
Sinusoidal 28
Normal All normal features
1 non-reassuring feature
Suspicious And
2 reassuring features
1 abnormal feature
Pathological OR
2 non-reassuring features

Regard the following as concerning characteristics of variable decelerations (atypical) :


lasting more than 60 seconds
reduced baseline variability within the deceleration
failure to return to baseline
biphasic (W) shape
no shouldering.
NICE FEB 2017
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THE END
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